Albert Eye Research Institute, Duke University, Durham, NC 27710, USA.
Neuron. 2011 Oct 6;72(1):101-10. doi: 10.1016/j.neuron.2011.07.030.
Dark and light adaptation of retinal neurons allow our vision to operate over an enormous light intensity range. Here we report a mechanism that controls the light sensitivity and operational range of rod-driven bipolar cells that mediate dim-light vision. Our data indicate that the light responses of these cells are enhanced by sustained chloride currents via GABA(C) receptor channels. This sensitizing GABAergic input is controlled by dopamine D1 receptors, with horizontal cells serving as a plausible source of GABA release. Our findings expand the role of dopamine in vision from its well-established function of suppressing rod-driven signals in bright light to enhancing the same signals under dim illumination. They further reveal a role for GABA in sensitizing the circuitry for dim-light vision, thereby complementing GABA's traditional role in providing dynamic feedforward and feedback inhibition in the retina.
视网膜神经元的暗适应和明适应使我们的视觉能够在很大的光强度范围内运作。在这里，我们报告了一种控制介导暗光视觉的杆状细胞驱动双极细胞的光敏感性和工作范围的机制。我们的数据表明，这些细胞的光反应通过 GABA(C)受体通道持续氯离子电流增强。这种致敏的 GABA 能输入受多巴胺 D1 受体控制，水平细胞作为 GABA 释放的可能来源。我们的发现将多巴胺在视觉中的作用从其在强光下抑制杆状细胞驱动信号的既定功能扩展到在暗光下增强相同信号的作用。它们进一步揭示了 GABA 在敏化暗光视觉电路中的作用，从而补充了 GABA 在视网膜中提供动态前馈和反馈抑制的传统作用。
